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在有丝分裂中,基因 A 相关激酶-6 减弱了压力超负荷诱导的蛋白激酶 B 通路的激活和心脏肥大。

Never in mitosis gene A related kinase-6 attenuates pressure overload-induced activation of the protein kinase B pathway and cardiac hypertrophy.

机构信息

Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, P. R. China; Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei Province, P. R. China.

Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, P. R. China.

出版信息

PLoS One. 2014 Apr 24;9(4):e96095. doi: 10.1371/journal.pone.0096095. eCollection 2014.

Abstract

Cardiac hypertrophy appears to be a specialized form of cellular growth that involves the proliferation control and cell cycle regulation. NIMA (never in mitosis, gene A)-related kinase-6 (Nek6) is a cell cycle regulatory gene that could induce centriole duplication, and control cell proliferation and survival. However, the exact effect of Nek6 on cardiac hypertrophy has not yet been reported. In the present study, the loss- and gain-of-function experiments were performed in Nek6 gene-deficient (Nek6-/-) mice and Nek6 overexpressing H9c2 cells to clarify whether Nek6 which promotes the cell cycle also mediates cardiac hypertrophy. Cardiac hypertrophy was induced by transthoracic aorta constriction (TAC) and then evaluated by echocardiography, pathological and molecular analyses in vivo. We got novel findings that the absence of Nek6 promoted cardiac hypertrophy, fibrosis and cardiac dysfunction, which were accompanied by a significant activation of the protein kinase B (Akt) signaling in an experimental model of TAC. Consistent with this, the overexpression of Nek6 prevented hypertrophy in H9c2 cells induced by angiotonin II and inhibited Akt signaling in vitro. In conclusion, our results demonstrate that the cell cycle regulatory gene Nek6 is also a critical signaling molecule that helps prevent cardiac hypertrophy and inhibits the Akt signaling pathway.

摘要

心脏肥大似乎是一种细胞生长的特殊形式,涉及增殖控制和细胞周期调节。NIMA(有丝分裂中从未出现,基因 A)相关激酶-6(Nek6)是一种细胞周期调节基因,可诱导中心粒复制,并控制细胞增殖和存活。然而,Nek6 对心脏肥大的确切影响尚未报道。在本研究中,通过 Nek6 基因缺陷(Nek6-/-)小鼠和 Nek6 过表达 H9c2 细胞的功能丧失和获得实验,阐明了促进细胞周期的 Nek6 是否也介导心脏肥大。通过胸主动脉缩窄(TAC)诱导心脏肥大,然后通过体内超声心动图、病理和分子分析进行评估。我们获得了新的发现,即 Nek6 的缺失促进了心脏肥大、纤维化和心功能障碍,这伴随着 TAC 实验模型中蛋白激酶 B(Akt)信号的显著激活。与此一致的是,Nek6 的过表达可防止血管紧张素 II 诱导的 H9c2 细胞肥大,并抑制体外 Akt 信号通路。总之,我们的结果表明,细胞周期调节基因 Nek6 也是一种关键的信号分子,有助于预防心脏肥大并抑制 Akt 信号通路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71be/3999101/2bfaefcb9dcd/pone.0096095.g001.jpg

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